Intro to EKG Interpretation - Overview of Tachyarrhythmias

hello everyone in today's video on EKG I'll be reviewing the basic types of tachyarrhythmias focusing on their EKG characteristics the specific learning objective is to be able to list the general mechanism ideologies and defining EKG characteristics of each of the six major forms of tachyarrhythmia future videos we'll cover some advanced tachyrhythmia topics such as how to differentiate the various forms of SVT how to differentiate V T from SVT with aberrancy the various forms of atrial flutter and more about V T in general for someone who is either completely new or relatively new to EKG interpretation I would consider there to be six different forms or categories of tachyarrhythmias a general cardiologist might consider there to be more like 15 or so and for an electrophysiologist there would be many more than that but for now let's consider just six in no particular order they are sinus tachycardia atrial fibrillation atrial flutter multifocal atrial tachycardia super ventricular tachycardia which is an umbrella term inclusive of more specific rhythms with confusing acronyms like avnrt and avrt along with something called atrial tachycardia and finally there is ventricular tachycardia which can be subdivided into monomorphic and polymorphic subtypes I'll go through each one at a time but while we're on the screen I want to point out that the first 5 rhythms on this list typically have a narrow QRS complex unless one of the following is present an underlying bundle branch block pre-excitation a condition in which a patient has an abnormal bundle of conductive tissue that connects the atria and ventricles bypassing the AV node although not strictly correct this is often used synonymously with wolff-parkinson-white or WPW syndrome use of drugs which prolong the QRS complex most notably class 1a and 1c antiarrhythmics such as procainamide and flick and ID respectively and the last profound hyperkalemia ventricular tachycardia on the other hand always has a wide QRS complex I'll first focus on sinus tachycardia the general mechanism of sinus tach is enhanced normal automaticity in which the heart's conductive system is simply responding normally to an extra cardiac stimulus this typically occurs as a consequence of stimulation of beta-1 adrenergic receptors by norepinephrine which is released at sympathetic nerve endings and by an epinephrine released into the systemic circulation by the adrenals stimulation of beta 1 receptors in the pacemaker cells of the sinus node cause them to spontaneously depolarize at a faster rate there are many ideologies of sinus tachycardia the only unifying theme to the ideologies is that with the exception of CHF exacerbations and possibly the idiopathic syndromes they otherwise are not primary disorders of the heart but rather path of physiologic states which result in increased activity of the sympathetic nervous system on EKG the hallmark features of sinus tachycardia are first that it is regular second the P waves are clearly discernible before each QRS complex with identical morphology to normal sinus rhythm sinus tach it develops over minutes to hours rather than over a few seconds and the rate is usually variable over time rather than being fixed the rhythm is atrial fibrillation usually abbreviated a fib the general mechanism of afib is something called micro reentry but the details of the specific mechanism is still debated and an area of active research all theories about the specific mechanism invoke multiple simultaneous chaotic waves of depolarization propagating through the atria with frequencies in excess of 500 beats of minutes though only a fraction of those impulses will pass through the AV node to depolarize the ventricles as a consequence of these chaotic depolarization waves there is no organized atrial contraction while sinus tach has ideologies it's more accurate to describe a fib as having risk factors the difference is that while just about every person who develops sepsis or hypoxemia or psychosis will get sinus tach not everyone who has hypertension or coronary disease ends up with afib these risk factors for afib can be divided into those which predisposed to afib by predisposing - left atrial stretch and dilation such as hypertension CHF mitral valve disease and coronary artery disease and then there are risk factors whose exact mechanism for increasing risk is unknown or incompletely known such as during the immediate post-op period following cardiac surgery stimulant or alcohol intoxication obstructive sleep apnea pulmonary embolism hyperthyroidism and hypomagnesemia although hypokalemia is widely believed to be a cause of afib to the best of my knowledge this hasn't been established yet in the literature an example of a fib it is the classic irregularly irregular rhythm meaning that it is both irregular and there is no repeating pattern to that irregularity the atrial activity as visible on EKG consists of irregular low amplitude undulations often called fibrillation waves or f waves with a lowercase F those undulations can sometimes be unusually prominent or seem more organized but as long as they are occurring at a very fast frequency and have variable morphology it is still best to consider the rhythm a fib unlike sinus tach which occurs gradually a fib develops very abruptly one moment the patient is in sinus rhythm and then he or she is instantaneously switched into afib like sinus rhythm though it too can have a rate that varies dramatically over time sometimes afib will fall into a tachycardic category sometimes the rate would be normal and rarely it will be bradycardic berta carnac afib implies severe AV node disease or an excessive dose of the medication that blocks the AV node atrial flutter is also a reentrant rhythm but in contrast to afib the specifics of most forms of a flutter are well worked out the most common reentrant pathway is a macroscopic counterclockwise circuit encircling the right atrium passing through the cable tricuspid Isthmus in which the Isthmus is the slow pathway of the reentrant circuit this form of flutter is thus called isthmus dependent flutter there are many other variations and subtypes of a flutter all of which have the unifying theme of macro reentry within one of the atria don't worry if you happen to have skipped the mechanisms of arrhythmia video and have no idea to what I'm referring when I mentioned reentrant circuits and slow pathways knowledge of the mechanism is not critical to diagnosing the rhythm from EKG when it comes to etiology x' and/or risk factors for a flutter any risk factor for afib particularly those associated with atrial dilation can generate the electrophysiologic substrate conducive for a flutter in other words unlike SVT which we'll talk about in a few minutes patients with a flutter are generally not thought to have been born with discrete well defined accessory pathways that predispose them to reentry but rather develop heterogeneity of the conductive properties of the atria over time that heterogeneity is almost always the result of some form of cardiac disease partly because the risk factors of afib and a flutter are essentially the same it should come as no surprise that patients commonly flip back and forth between the two rhythms in addition cardiac surgery and percutaneous afib ablations are significant risk factors for developing unusual forms of flutter what are the EKG characteristics of a flutter the ventricular activity that is the pattern of QRS complexes in a flutter can either be regular regularly irregular or irregularly irregular atrial activity consists of regular saw tooth wave forms most prominent in 2-3 and a VF along with upright deflections in v1 which occur at a rate of 240 to 340 beats per minute the rate of atrial activity often referred to as a flutter rate is commonly right at 300 beats per minute exactly this very rapid atrial activity is sometimes referred to as an F wave with a capital F rate slower than 300 are typically seen in patients with very enlarged atria or those on class-one antiarrhythmics rates faster than 300 are typical only for patients with unusual flutter circuits the way I think about this is that the speed of a reentrant rhythm is largely dependent upon the physical size of the reentrant circuit therefore as long as a patient has the same location as typical for the circuit in the right atrium as long as the right atrium is normal in size it makes sense for the flutter rate to be about the same usually 50% or more of atrial impulses are blocked by the AV node so for example if the flutter rate in the atria is 300 beats per minute but every other atrial impulse is blocked by the AV node because of the AV nodes refractory period then the overall ventricular rate will be 150 beats per minute like a fib a flutter develops abruptly and finally the rate can vary over time and can demonstrate abrupt discrete incremental changes associated with abrupt changes in the degree of AV block let me show you three variations of a flutter first is a regular ventricular response in this case a consequence of two-to-one AV block producing a ventricular rate of 150 it's not very common but on occasion AV block and a flutter can manifest an interesting pattern in which for 2 1 av block alternates with 2 to 1 AV block and repetitive pattern resulting in a regularly irregular ventricular response if the atrial rate is around 300 this pattern will result in a ventricular rate of around 100 very astute viewers might note that in this particular example the second QRS complex in each pair here comes ever so slightly late for a pure 4 to 1 alternating with 2 to 1 block which is fairly common to see in this pattern and a flutter can also have an irregularly irregular pattern which can mimic a fib if the flutter waves are very small where if the rhythm is being evaluated on its lemon tree monitor which often do not capture atrial activity with sufficient resolution a minute ago I mentioned that a flutter can demonstrate discrete incremental changes in rates let me show you what I was talking about most modern telemetry systems have the capability of graphing heart rates as a function of time here's how that graph might look for a page who starts in sinus rhythm and then develops flutter so the patient is chugging along with a sinus rate in the 60s with a little completely normal rate variability and then suddenly converts into flutter at first maybe the patient is in two to one block at 150 beats per minute for let's say 30 minutes then appropriately converts the flutter with four to one block at 75 beats per minute then there is a brief period of variable block before the patient develops four to one block alternating with two to one then some variable block again before ending up in consistent two to one block and then snap the patient spontaneously converts back to sinus rhythm again with the sinus rhythms intrinsic rate variability this results in a pattern of incremental discrete changes in heart rate occasionally a student or resident can look like a superstar by suggesting flutter from only looking at a similar rate as a function of time graph before having the opportunity to see an actual rhythm recording the next rhythm is called multifocal atrial tachycardia abbreviated ma T of the six categories of tachyarrhythmias this is the least common the general mechanism of ma T is unknown but it's believed to be triggered activity as with the previous mention of reentry if you're not familiar with the term triggered activity don't worry knowledge of the physiological concept is absolutely not necessary to accurately diagnose the rhythm ma T is solely seen in two general situations first acute pulmonary disease which can be a COPD exacerbation pneumonia or PE and second in a CHF exacerbation multiple studies have suggested a correlation between use of theophylline and MIT one that goes beyond just the association with COPD exacerbations alone there's also a common belief that hypokalemia and hypomagnesemia can contribute to the development m80 but this remains unproven there are three EKG characteristics that define m80 first it is an irregularly irregular rhythm second there are three or more distinctly different p-wave morphologies and the third there is no one predominant p-wave morphology if there was one predominant morphology and more accurate description of the rhythm would likely be sinus tach with frequent multifocal premature atrial contractions let's look for those different P waves in this example here's the first does this morphology show up later in the rhythm strip yes I think it does right here then here's the next P wave morphology which seems to recur here and this unusual appearing sharp negative P wave appears to be the third morphology which I think gets repeated here here and here though some of these may actually be different and here's the last unique morphology here and here so in this six second strip there are at least four maybe more morphologies and hopefully you agree that none of them seem to be predominant over the others the fifth category of tachyarrhythmia is supraventricular tachycardia abbreviated SVT this is a strange term that doesn't exactly mean what you might guess from its name after all sinus tach would seem to be a super ventricular tachycardia since it originates from above the ventricles in medicine however particularly cardiology this umbrella term is used specifically for any tachyarrhythmia that originates from above the ventricles and is neither sinus tach a fib a flutter or m80 the overwhelming majority of SVT's are one of three rhythms avnrt avrt or atrial tachycardia for someone just starting out with EKG interpretation please do not worry about the difference between the SVT s were worried about how to distinguish one from another it's very nuanced and often experienced cardiologists have difficulty with this task I strongly recommend considering all SVT's to represent one diagnosis at this point however since the SB T's are a diverse group of arrhythmias collectively they can evoke any mechanism though overall reentry is the most common the etiology of the vast majority of SVT's is an anatomic anomaly either re-entrant circuit or a tiny island of hyper excitable tissue in the atria in addition a small fraction of cases of atrial tachycardia specifically can be caused by digoxin toxicity despite their varied mechanisms all SVT share some EKG features they are all highly regular the rates tend to be in the neighborhood of 150 to 200 beats per minute but can rarely be as slow as 120 or as fast as 250 the P waves may come before the QRS after the QRS or not be visible at all meaning they occur simultaneous as a QRS when visible the P waves usually have an abnormal morphology consistent with either an ectopic atrial focus or retrograde atrial conduction most though not all SBTs begin abruptly and the rate is usually but not always very constant here are three examples of SVT s in this case there is a very short nine beat run of an SVT in which the P wave comes before the QRS complex notice how the P wave morphology during the arrhythmia differs from that when the patient is presumably in normal sinus here is an example in which the p-wave comes after the QRS complex and notice that it has an upside-down morphology if this were a recording of an inferior lead such as 2 3 or a BF which this could be we would call those retrograde p-waves meaning that the wave of depolarization in the atria is moving in an inferior to superior direction away from the AV node and towards the sinus node and here's an example in which the P waves are not visible at all the significance of where the P waves are occurring during an SVT will be discussed in the future video focused solely on the SVT s the final rhythm I'll discuss today is the most dangerous and fortunately usually the most obvious ventricular tachycardia abbreviated VT VT can be due to any mechanism of a rhythmic emesis there are many many causes of VT the most notable of which is a myocardial scar from prior mi which can set up a macro reentry circuit around the infarcted tissue VT commonly has a single QRS morphology and is usually regular this is called monomorphic VT it is common for the first handful of beats of a monomorphic VT to show some irregularity VT can rarely have multiple QRS morphologies in which case it's usually irregular this is called polymorphic VT VT always has a wide QRS complex and almost always is greater than 140 milliseconds in width and though it's a minority of VTE kgs which show this if you see evidence of AV dissociation fusion beats or capture beats when these are present it is essentially diagnostic of VT for those viewers who are unfamiliar with the term AV dissociation this refers to the situation in which the atria and ventricles are not communicating with one another on EKGs this is evident as P waves and QRS complexes occurring different rates and which appear completely independent of one another av dissociation is much better seen in complete heart block and even when present in VT it is usually only a rare dissociated P wave that will be visible between the wide rapid QRS complexes here's an example of monomorphic VT this little bump on the down slope of the second T wave is suspicious for a dissociated P wave in other words evidence of a B dissociation and here's a classic example of the much rarer polymorphic VT this is its most well-known subtype something called toursad dip want which is almost universally caused by a prolonged QT interval so those are the six basic types of tachyarrhythmias as I said at the beginning of the video some of these specifically SVT VT and atrial flutter have numerous subtypes and variations that you can worry about at a later stage of training at this point I recommend proceeding to my next EKG video entitled how to identify almost any tachyarrhythmia with six easy questions you

Channel: Strong Medicine

Views: 264,593

Keywords: ekg, ecg, Electrocardiography (Invention), ekg interpretation, ventricular tachycardia, supraventricular tachycardia, Supraventricular Tachycardia (Disease Or Medical Condition), Cardiac Arrhythmia (Disease Or Medical Condition), Ventricular Tachycardia (Disease Or Medical Condition), sinus tachycardia, tachycardia, tachyarrhythmia, multifocal atrial tachycardia, torsades de pointes, reentry, atrial fibrillation, atrial flutter

Id: iT3cVVK74tU

Length: 23min 17sec (1397 seconds)

Published: Mon Apr 28 2014